Similarities and differences in the postjunctional role for neuropeptide Y in sympathetic vasomotor control of large vs. small arteries of rabbit renal and ear vasculature.

Neuropeptide Y (NPY) coexists and is coreleased with norepinephrine (NE) from postganglionic sympathetic nerves. A correlation between the peripheral vascular effects of NPY and the diameter of blood vessels has been proposed: NPY induces a stronger contraction in small arteries, whereas the potentiation of the contractile responses induced by other vasoconstrictors, such as NE, seems to be restricted to larger arteries where NPY exhibits little or no direct contractile activity. The purpose of the present study was to systematically characterize in vitro the contractile effects of NPY per se and the effects of NPY on contractions evoked by exogenous NE in sequential artery segments of diminishing diameter from rabbit ear and kidney. The ability of NPY to evoke vasoconstriction increased with decreasing arterial diameter. The ability of NPY to potentiate exogenous NE-induced force of contraction was restricted to larger arteries where NPY had little or no contractile effect. The velocity of NE EC50-induced force development was augmented in the presence of NPY in all ear and intrarenal arteries. This is the first report of dissociation between the potentiation of exogenous NE-induced force of contraction by NPY and the increase in velocity of NE-induced force development by NPY. If, as has been suggested by other investigators, increased rate of contraction results in potentiation of contractile responses to short trains of adrenergic nerve stimulation, this latter finding suggests that a potentiation of contractile responses to short trains of adrenergic nerve stimulation occurs at all levels of the ear and intrarenal arterial vasculature.